Photodynamic agents which exhibit virucidal activity have been investigated for use with cellular blood components, using platelets as a model cell system. We examined the effect of the photosensitizer, merocyanine 540 (MC), +/- 450-600nm light on platelets and the influence of albumin on the virucidal activity of MC. Platelet function was assessed as the aggregation response to thrombin (0.035-0.10 U/mL) following treatment of washed platelets (+/- albumin (<-5%)) with MC (</=72ug/mL) +/- light (450-600nm, 18 joules (J)/cm2). Platelets treated with MC (24 ug/mL) and light in the presence of low concentrations of albumin (<0.35%) aggregated spontaneously without thrombin stimulation. A normal aggregation response of MC-treated platelets to thrombin was maintained only upon addition of 5% albumin to the medium. Platelet activation without added agonist served as an indicator of photodamage to the platelets and was demonstrated by the release of serotonin. Platelets treated with MC (15 ug/mL) in albumin-free medium released 51% serotonin in the dark and 93% serotonin upon light exposure. The addition of albumin (>-2.5%) to the platelet suspension medium fully protected the platelets against these effects of MC and light. Since inactivation of viruses in blood products is likely to be performed in a protein-rich medium, we assessed the affect of albumin (5%) on the photosensitized killing of several marker viruses, including bacteriophage 06, bacteriophage PM2 and herpes simplex virus. Both 06 and HSV are lipid enveloped, viruses and were extremely sensitive to MC (15 micro-g/mL) and light with D0s of 0.28J/cm2 and 0.011 J/cm2, respectively. PM2, with internal lipid, was much less sensitive to dye and light treatment and exhibited a D0 of 3.26 J/cm^2. Inactivation of 06 and PM2 (by 18 J/cm2) was completely prevented by 5% albumin. Under these conditions, HSV was still inactivated, but with an increased Do (2.1 J/cm2). Therefore, concentrations of albumin which protect platelets from photodamage significantly reduce the antiviral activity of MC. The potential treatment of cellular blood products with MC may be limited by its inability to fully inactivate viruses under conditions required to maintain platelet function. Results of these studies have been submitted for publication to Transfusion (July, 1990) and have been presented at the annual meetings of the American Association of Blood Banks (Oct. 1989) and the International Photodynamic Association (July 1990).